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Query: UMLS:C0231835 (tachypnea)
 2,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A three-day-old female infant was transferred to the Pediatric Intensive Care Unit with chief presenting problems of progressive change of cyanosis and respiratory distress. Physical examination revealed tachypnea, acrocyanosis, hepatomegaly, undetectable pulse of extremities and oozing over the place of venous puncture. Chest roentgenograms revealed slight cardiomegaly; other X-rays were within normal limits. Complete electrocardiograms showed right axis deviation and right ventricular hypertrophy. Because of an impression of neonatal sepsis, the patient was put in an incubator with oxygen and antibiotics were given. Persistent anuria appeared associated with sighs of cardiac and renal failure; the ventilator was applied; dopamine and lasix were also given. Unfortunately, the cyanosis worsened progressive. Despite several attempts at resuscitations, the infant expired eight hours later. Pathology disclosed the heart size as normal; hypoplasia of ascending aorta as 0.4 cm in diameter; a PDA with 1 cm in diameter; a diminutive bean-sized left ventricle; hypertrophy of right ventricle and atresias of aortic and mitral valves. There was no evidence of septicemia.
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PMID:[Hypoplastic left heart syndrome due to aortic and mitral atresias: report of one case]. 263 9

Although the conditions that cause hypoglycemia in adults may also be present in infants and children, there are many entities unique to the pediatric age group. This reflects the delicate balance that exists in the newborn and young child between glucose production and utilization. During fasting in infants and children, hepatic glucose production is normally two to three times that of adults when expressed on the basis of weight. In the newborn and young infants, hypoglycemia usually presents with irritability, feeding difficulties, lethargy, cyanosis, tachypnea, and/or hypothermia rather than the typical adrenergic or neuroglucopenic symptoms seen in the adult. The hypoglycemia may be due to abnormalities in hormone secretion, substrate interconversion, or mobilization of metabolic fuels. The hypoglycemia associated with hyperinsulinemia may be transient neonatal, sustained, or drug-induced. Inborn errors of metabolism caused by enzymatic defects are responsible for hypoglycemia associated with abnormalities of production and utilization of metabolic fuels. These can involve carbohydrate, protein, and fat metabolism. In addition, there may be acquired or transient defects in carbohydrate metabolism secondary to other diseases or ingestion of certain substances. Finally ketotic hypoglycemia appears to be due to abnormalities in substrate availability. A variety of tests are useful for establishing the etiologic basis of the hypoglycemia, and the appropriate treatment depends upon the underlying cause.
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PMID:Hypoglycemia in infants and children. 264 28

In summary, HAPE is a potentially fatal form of noncardiogenic PE seen in a small number of individuals visiting above 9,000 ft in elevation. The pathophysiology is uncertain but is probably due, at least in part, to hydrostatic and capillary permeability abnormalities of the pulmonary vascular bed in response to hypobaric hypoxia. A subclinical form above 14,000 ft is common (15% to 23% incidence), but the incidence of HAPE itself is unclear. Possible risk factors include rapid ascent, strenuous activity on arrival, reascent to altitude by highlanders after a short stay lower, previous HAPE, cold, respiratory tract infections, sedation, youth, and the peripheral edema of AMS. Clinical presentation is similar to that of pneumonia: tachypnea, tachycardia, cyanosis, cough, fever, and chest discomfort. Symptoms often worsen with sleep. WBC count is usually elevated, and arterial blood gases reveal a respiratory alkalosis and an alarmingly low hemoglobin saturation. Chest radiographs reveal bilateral patchy infiltrates. Radiographic findings are dissimilar to those from cardiogenic PE. Differential diagnosis includes pneumonia, PE and HAB. Treatment modalities include early descent, bed rest, oxygen therapy, and EPAP. Mortalities range from 4% to 27% depending on the rapidity of descent and evacuation.
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PMID:High-altitude pulmonary edema: a collective review. 266 Aug 18

It is important to define clinical signs that can be used to identify children who have a high risk of dying from pneumonia so that these children can be given more intensive therapy. We prospectively studied 748 children in Papua New Guinea who had severe pneumonia, as defined by the World Health Organization. There was a very high mortality in children with a prolonged illness, severe roentgenogram changes, cyanosis, leukocytosis, hepatomegaly or inability to feed, and there was a trend toward a higher mortality in children with grunting or severe chest indrawing. Afebrile malnourished children had a particularly high mortality, but afebrile children had an increased mortality only if they were malnourished, and malnourished children had an increased mortality only if they were afebrile. Mortality was not increased in very young children or in children with tachypnea or tachycardia. The World Health Organization has suggested that most children with pneumonia in developing countries can be treated with penicillin but has recommended that children who are cyanotic or too sick to feed be treated with chloramphenicol because of their high risk of dying; our findings confirm that children who are cyanotic or too sick to feed have a very high risk of dying from pneumonia.
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PMID:Clinical signs that predict death in children with severe pneumonia. 269 26

Following diverse insults, patients may develop a high permeability lung oedema which results in tachypnoea, cyanosis, hypoxaemia, and pan-lobar infiltrates on the chest radiograph. Although a variety of interventional therapies have been evaluated, none has been found effective, and current treatments are entirely supportive. Recently, cellular and biochemical analyses of bronchoalveolar lavage fluid have disclosed abnormalities which suggest that acute inflammatory events and surfactant abnormalities are present in the lungs of patients with adult respiratory distress syndrome (ARDS). The similarities to abnormalities seen in neonates with respiratory distress syndrome are striking. Treatment of those infants with surfactant replacement has been of both short-term and long-term benefit. Therefore, it is rational to investigate the benefits which surfactant administration may have for patients with ARDS. We present an overview of ARDS, and our initial experience with surfactant replacement in three patients.
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PMID:The adult respiratory distress syndrome: first trials with surfactant replacement. 274 81

The patient was a 63-days-old boy who was admitted to our hospital because of moderate cyanosis and tachypnea. After admission, severe respiratory distress and emphysematous change of the right lung on the chest X-ray developed progressively. Echocardiogram and angiocardiogram demonstrated that a tetralogy of Fallot associated with right aortic arch and absence of pulmonary valve, and revealed remarkably dilated ascending aorta which compressed the right pulmonary artery and bronchus. Therefore, the emergency operation in that the ascending aorta was suspended to the 2nd rib was performed through a right thoracotomy. After surgery, his respiratory distress and emphysema of the right lung completely disappeared. To our knowledge, this is the 2nd reported case in which suspension of ascending aorta was successfully performed for pulmonary complication in congenital cardiovascular anomalies as this patient.
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PMID:[A case report of compression of right pulmonary artery and bronchus by aneurysmal dilated ascending aorta in tetralogy of Fallot--suspension of ascending aorta]. 276 13

A two-month-old boy with anomalous origin of the left anterior descending coronary artery (AOLAD), aortic stenosis (AS), coarctation of the aorta (CoA) and patent ductus arteriosus (PDA) is reported. Tachypnea was observed since birth. When he arrived at our hospital, congestive heart failure, cyanosis of his lower extremities and weak femoral pulses were observed. Radiography revealed cardiomegaly and pulmonary congestion. ECG showed low voltage in all leads, ST elevation in leads II, aVF, V5,6 and abnormal Q waves in V5,6. The tentative diagnosis by two-dimensional echocardiography (2DE) was AS, CoA, PDA, pulmonary hypertension and pericardial effusion. The abnormal coronary artery was visualized as originating from the left anterior wall of the pulmonary artery, coursing between the pulmonary artery and left atrial appendage. A definitive diagnosis of AOLAD were made by angiography. Aortic reconstruction using an artificial graft for CoA and PDA ligation was performed first. He died of myocardial infarction while waiting for his second operation for AOLAD and AS. Autopsy confirmed the aforementioned diagnoses as well as old and recent infarction of the myocardium. AOLAD is a rare congenital malformation, only six cases of which have been reported. Moreover, AOLAD complicated by other anomalies had not been previously reported. This is the first such reported case.
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PMID:[Anomalous origin of the left anterior descending coronary artery from the pulmonary artery associated with other anomalies: a case report]. 281 50

The most common congenital cardiac defect is VSD. This malady accounts for 20 to 30 per cent of all congenital cardiac defects and is representative of a cardiac lesion that increases pulmonary blood flow. Although lesions, which increase pulmonary blood flow, may vary in incidence, they frequently have common symptomatology. Over time, congestive heart failure becomes a problem. Poor respiratory status leads to weight loss, poor feeding, and failure to thrive. If unrepaired, the child often presents with cyanosis and tachypnea. The history may include frequent respiratory infections, exercise intolerance, generalized malaise, or fatigue. In spite of poor weight gain, the child may be edematous and have a large liver. Definitive diagnosis of each lesion may be made by echocardiogram, cardiac catheterization, or both. With these data and a detailed history, treatment and management decisions are determined. In most cases, as the child gets older, symptoms become more evident. This is the result of high pulmonary pressure. High pressure over time causes a thickening of the alveolar tissue, which decreases the permeability of the alveolar membranes for gas exchange. Lung changes can become irreversible, but it is unusual for irreversible changes to occur before 1 year of age. All the lesions described in this article are amendable to primary repair before 1 year of age, affording the best functional results. Postoperative nursing care includes management of persisting CHF and PVR while maintaining adequate cardiac output. Many factors, including electrolyte balance, nutritional status, conduction disturbances, stress, and parental anxiety, influence the management of these infants. The outcome depends greatly on the assessment skill of a highly competent cardiac intensive care nurse and an environment conducive to collaborative practice.
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PMID:Caring for patients with lesions increasing pulmonary blood flow. 281 77

A newborn with mediastinal teratoma developed tachypnea and cyanosis within the first hours of life. Chest x-ray revealed a subtotal opacification of the left hemithorax, which at first was suspected to be caused by a cardiomegaly. Ultrasound examination demonstrated a large mass in the left hemithorax with multiple echo-free areas. This finding was suspicious for a mediastinal teratoma. The tumor which was originating from the mediastinum was apple-sized and could be resected totally by thoracotomy. Histology revealed a cystic teratoma covered with normal thymus tissue.
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PMID:[Mediastinal teratoma in a newborn infant]. 304 9

A patient with acute hyperleukocytotic myelogenous leukemia who presented with acute respiratory distress is reported. Clinical manifestations included dyspnea, tachypnea, hyperventilation, and cyanosis. Blood gas analysis revealed hypoxemia, hypocapnia, and metabolic acidosis. Chest X-ray and perfusion lung scanning were normal. Pulmonary leukostasis syndrome (PLS) was later confirmed at autopsy. In a patient with hyperleukocytosic from acute nonlymphocytic leukemia and respiratory distress, a normal perfusion lung scintigraph should make one consider the PLS.
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PMID:Acute respiratory failure in hyperleukocytotic acute myeloid leukemia: the role of perfusion lung scintigraphy. 316 47


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